Addiction experts in psychiatry, chemistry, pharmacology, forensic science, epidemiology, and the police and legal services engaged in delphic analysis regarding 20 popular recreational drugs. GHB was ranked 15th in dependence, 19th in physical harm, and 14th in social harm.[18]

GHB is a central nervous system depressant used as an intoxicant,[19] although it produces a stimulant effect at lower doses due to its action on the GHB receptor.[citation needed] It has many street names, including G, Liquid G, Liquid X, Liquid E,[20]Georgia Home Boy, Juice, Mils, and Fantasy.[citation needed] Its effects have been described anecdotally as comparable with ethanol (alcohol) and MDMA use, such as euphoria, disinhibition, enhanced libido and empathogenic states. At higher doses, GHB may induce nausea, dizziness, drowsiness, agitation, visual disturbances, depressed breathing, amnesia, unconsciousness, and death. When death is associated with GHB, it is sometimes in conjunction with other drugs, such as alcohol or benzodiazepine which influence the same neurotransmitter (gamma-aminobutyric acid, GABA). The effects of GHB can last from 1.5 to 4 hours, or even longer if large doses have been consumed.[21] Consuming GHB with alcohol is dangerous as it can lead to respiratory arrest and vomiting in combination with unrouseable sleep, a potentially lethal combination.[22][23]

In general, the doses used recreationally are between 0.5 g and 3 g.[citation needed] When used as a recreational drug, GHB may be found as the sodium or potassium salt, which is a white crystalline powder, or as GHB salt dissolved in water to form a clear solution. The sodium salt of GHB has a salty taste.[21] Other salt forms such as calcium GHB and magnesium GHB have also been reported, but the sodium salt is by far the most common.

Some chemicals convert to GHB in the stomach and blood stream. γ-Butyrolactone (GBL) is one such prodrug. Other prodrugs include 1,4-butanediol (1,4-B). There may be additional toxicity concerns with these precursors. 1,4-B and GBL are normally found as pure liquids, though they may be mixed with other more harmful solvents when intended for industrial use, e.g., as paint stripper or varnish thinner.

GHB can be easily manufactured with very little knowledge of chemistry, as it only involves the mixing of its two precursors, GBL and an alkali hydroxide, such as sodium hydroxide, to form the resulting GHB salt. Due to the ease of manufacture and the availability of its precursors, it is not mainly produced in illicit laboratories like most other synthetic drugs, but in private homes by low level producers instead. While available as a prescription for rare and severe forms of sleep disorders such as narcolepsy in some other countries, notably most of Europe, GHB was banned in the U.S. by the FDA in 1990. However, on 17 July 2002, GHB was approved for treatment of cataplexy, often associated with narcolepsy. GHB is "colourless and odorless".[24]

GHB is often taken because users find that it enhances their experiences of being in a club, party, or rave; small doses of GHB can act as a stimulant and aphrodisiac. GHB is sometimes referred to as liquid ecstasy, lollipops, liquid X or liquid E due to its tendency to produce euphoria and sociability and its use in the dance party scene.[25] Despite these nicknames, GHB and MDMA (ecstasy) have entirely separate chemical and pharmacological modes of action.

As certain succinate salts have been shown to elevate growth hormone in vitro,[28] and because GHB is metabolized into succinate some people have suggested this plays a role in the growth hormone elevations from GHB. There is however currently no evidence to show that succinate plays any role in the growth hormone elevations from GHB.

GHB is primarily known to the general public as a date rape drug. The drug is sometimes used to numb the other person, making it easier to rape them. When unobtrusively administered in a drink the victim will quickly feel groggy and sleepy, and upon recovery may have an impaired ability to recall memories of events that occurred during the period of intoxication. Consequently, the evidence and the identification of the perpetrator of rape is often difficult. However, a survey in the Netherlands shows that the proportion of GHB in rape cases is greatly overestimated by the media.[29]

Like alcohol and potent benzodiazepines such as flunitrazepam (Rohypnol), GHB has been labeled as a date rape drug.[4] The sodium form of GHB has an extremely salty taste but, as it is colourless and odorless,[24] it has been described as "very easy to add to drinks"[24] that mask the flavor. GHB produced as a sodium salt (sodium oxybate) may provide a noticeable salty character to the drink, though individual sensitivity to the taste of salt varies.[30] GHB can also be produced as different salts, some of which do not have a taste as distinctive as the sodium salt (e.g., magnesium oxybate), or much less commonly in the unstable free-acid form.[31]

GHB has been used in cases of drug-related sexual assault, usually when the victim is vulnerable due to intoxication with a sedative, generally alcohol.[32] It is difficult to establish how often GHB is used to facilitate rape as it is difficult to detect in a urine sample after a day, and many victims may only recall the rape some time after this,[33][34] although GHB can be detected in hair.[35] Hair testing can be a useful tool in court cases or for the victim's own information.[36] Over-the-counter urine test kits only test for date rape drugs that are benzodiazepines, and GHB is not a benzodiazepine. To detect GHB in urine, the sample must be taken within four hours of GHB ingestion, and cannot be tested at home.[37] GHB can be detected in hair for months after GHB ingestion. Other drugs, such as muscle relaxers (Carisoprodol for example), are sometimes mixed with GHB. Therefore, it can be beneficial to request that the hair sample be tested for multiple drugs.

There have been several high-profile cases of GHB as a date rape drug that received national attention in the United States. In early 1999 a 15-year-old girl, Samantha Reid of Rockwood, Michigan, died from GHB poisoning. Reid’s death inspired the legislation titled the "Hillory J. Farias and Samantha Reid Date-Rape Drug Prohibition Act of 2000." This is the law that made GHB a schedule 1 controlled substance.[38]

In 2007 Germs drummer Don Bolles was arrested by Orange County, California police after his bottle of Dr. Bronner's Soap field tested positive for GHB; more sophisticated tests yielded negative results and he was released after five days.[39]

In the Netherlands GHB is illegal since January 1, 2002 under the Opium Act, previously under the Law on Medicines. Until May 7, 1996 the drug was available as a legal chemical. The Healthcare Inspectorate has sales prohibited by the Law on Medicines. In order to circumvent the ban on GHB, do it yourself packages were put on the market with which oneself could easily make GHB. These contained the basic raw materials to be mixed as well as instructions in order (in the proper proportions). The main ingredients for homemade GHB are still (separately) freely available commercially in the Netherlands (GBL (gamma-butyrolactone) or 1,4-butanediol, which is used as the alkaline industrial cleaning agent, sodium hydroxide, which can be found in drain cleaner, and distilled water or ethanol). Since 2005, GHB is medically used under the brand name Xyrem for the treatment of narcolepsy with cataplexy. In 2011 the party drug was placed on the list of hard drugs by the Dutch government, making it illegal other than for medical use prescribed by a doctor.[40][41] Also it is in addiction clinics used during detoxification of GHB in a reduction schedule to prevent severe withdrawal symptoms.

A 2006 study suggested that there was "no evidence to suggest widespread date rape drug use" in the UK and that less than 2% of cases involved GHB while 17% involved cocaine.[42][43]

In humans, GHB has been shown to reduce the elimination rate of alcohol. This may explain the respiratory arrest that has been reported after ingestion of both drugs.[44] A review of the details of 194 deaths attributed to or related to GHB over a ten-year period found that most were from respiratory depression caused by interaction with alcohol or other drugs.[45]

One publication has investigated 226 deaths attributed to GHB.[46] Of 226 deaths included, 213 had a cardiorespiratory arrest and 13 had fatal accidents. Seventy-one deaths (34%) had no co-intoxicants. Postmortem blood GHB was 18–4400 mg/L (median=347) in deaths negative for co-intoxicants.

One report has suggested that sodium oxybate overdose might be fatal, based on deaths of three patients who had been prescribed the drug.[47] However, for two of the three cases, post-mortem GHB concentrations were 141 and 110 mg/L, which is within the expected range of concentrations for GHB after death, and the third case was a patient with a history of intentional drug overdose.[48] The toxicity of GHB has been an issue in criminal trials, as in the death of Felicia Tang, where the defense argued that death was due to GHB, not murder.

GHB is produced in the body in very small amounts, and blood levels may climb after death to levels in the range of 30–50 mg/L.[49] Levels higher than this are found in GHB deaths. Levels lower than this may be due to GHB or to postmortem endogenous elevations.

A UK parliamentary committee commissioned report found the use of GHB to be less dangerous than tobacco and alcohol in social harms, physical harm and addiction.[50]

Although there have been reported fatalities due to GHB withdrawal, reports are inconclusive and further research is needed.[56] A common problem is that GHB does not leave traces in the body after a short period of time, complicating diagnosis and research.[57] Addiction occurs when repeated drug use disrupts the normal balance of brain circuits that control rewards, memory and cognition, ultimately leading to compulsive drug taking.[58][59]

Rats forced to consume massive doses of GHB will intermittently prefer GHB solution to water but, after experiments on rats, it was noted that "no rat showed any sign of withdrawal when GHB was finally removed at the end of the 20-week period" or during periods of voluntary abstinence.[60][61]

GHB has also been associated with a withdrawal syndrome of insomnia, anxiety, and tremor that usually resolves within three to twenty-one days.[19][56][62] The withdrawal syndrome can be severe producing acute delirium and may require hospitalization in an intensive care unit for management.[19] Management of GHB dependence involves considering the person's age, comorbidity and the pharmacological pathways of GHB.[63] The mainstay of treatment for severe withdrawal is supportive care and benzodiazepines for control of acute delirium, but larger doses are often required compared to acute delirium of other causes (e.g. > 100 mg/d of diazepam). Baclofen has been suggested as an alternative or adjunct to benzodiazepines based on anecdotal evidence and some animal data.[64] However, there is less experience with the use of baclofen for GHB withdrawal, and additional research in humans is needed. Baclofen was first suggested as an adjunct because benzodiazepines do not affect GABAB receptors and thus have no cross-tolerance with GHB while baclofen, which works via GABAB receptors, is cross-tolerant with GHB and may be more effective in alleviating withdrawal effects of GHB.[65]

GHB withdrawal is not widely discussed in textbooks and some psychiatrists, general practitioners, and even hospital emergency physicians may not be familiar with this withdrawal syndrome.[66]

Overdose of GHB can sometimes be difficult to treat because of its multiple effects on the body.[3][67][68] GHB tends to cause rapid unconsciousness at doses above 3500 mg, with single doses over 7000 mg often causing life-threatening respiratory depression, and higher doses still inducing bradycardia and cardiac arrest. Other side-effects include convulsions (especially when combined with stimulants), and nausea/vomiting (especially when combined with alcohol).[19]

The greatest life threat due to GHB overdose (with or without other substances) is respiratory arrest.[19][69] Other relatively common causes of death due to GHB ingestion include aspiration of vomitus, positional asphyxia, and trauma sustained while intoxicated (e.g., motor vehicle accidents while driving under the influence of GHB).[citation needed] The risk of aspiration pneumonia and positional asphyxia risk can be reduced by laying the patient down in the recovery position. People are most likely to vomit as they become unconscious, and as they wake up. It is important to keep the victim awake and moving, who must not be left alone due to the risk of death through vomiting. Frequently they will be in a good mood but this does not mean they are not in danger. GHB overdose is a medical emergency and immediate assessment in an emergency department is needed.

Convulsions from GHB can be treated with the benzodiazepinesdiazepam or lorazepam.[19] Even though these benzodiazepines are also CNS depressants, they primarily modulate GABAA receptors whereas GHB is primarily a GABAB receptor agonist, and so do not worsen CNS depression as much as might be expected.[citation needed]

Because of the faster and more complete absorption of GBL relative to GHB, its dose-response curve is steeper, and overdoses of GBL tend to be more dangerous and problematic than overdoses involving only GHB or 1,4-B. Any GHB/GBL overdose is a medical emergency and should be cared for by appropriately trained personnel.

A newer synthetic drug SCH-50911, which acts as a selective GABAB antagonist, quickly reverses GHB overdose in mice.[70] However, this treatment has yet to be tried in humans, and it is unlikely that it will be researched for this purpose in humans due to the illegal nature of clinical trials of GHB, and the lack of medical indemnity coverage inherent in using an untested treatment for a life-threatening overdose.[original research?]

GHB may be quantitated in blood or plasma to confirm a diagnosis of poisoning in hospitalized patients,[19] provide evidence in an impaired driving arrest or to assist in a medicolegal death investigation. Blood or plasma GHB concentrations are usually in a range of 50–250 mg/L in persons receiving the drug therapeutically (during general anesthesia), 30–100 mg/L in those arrested for impaired driving, 50–500 mg/L in acutely intoxicated patients and 100–1000 mg/L in victims of fatal overdosage. Urine is often the preferred specimen for routine drug abuse monitoring purposes. Both γ-butyrolactone (GBL) and 1,4-butanediol are converted to GHB in the body.[71][72][73]

In January 2016, it was announced scientists had developed a way to detect GHB, among other things, in saliva.[74]

Cells produce GHB by reduction of succinic semialdehyde via succinic semialdehyde reductase (SSR). This enzyme appears to be induced by cAMP levels,[75] meaning substances that elevate cAMP, such as forskolin and vinpocetine, may increase GHB synthesis and release. Conversely, endogeneous GHB production in those taking valproic acid will be inhibited via inhibition of the conversion from succinic acid semialdehyde to GHB. It is important to note, however, that direct administration of GHB or endogenous GHB already present in the body will not be affected by valproic acid.[76] People with the disorder known as succinic semialdehyde dehydrogenase deficiency, also known as γ-hydroxybutyric aciduria, have elevated levels of GHB in their urine, blood plasma and cerebrospinal fluid.[77]

The precise function of GHB in the body is not clear. It is known, however, that the brain expresses a large amount of receptors that are activated by GHB.[78] These receptors are excitatory and not responsible for the sedative effects of GHB – they have been shown to elevate the principal excitatory neurotransmitter—glutamate.[79] The benzamide antipsychotics—amisulpride, sulpiride—have been shown to bind to this receptor in vivo.[80] Other antipsychotics were tested and were not found to have an affinity for this receptor.

It is a precursor to GABA, glutamate, and glycine in certain brain areas.[81]

GHB has neuroprotective properties and has been found to protect cells from hypoxia.[82]

GHB is also produced as a result of fermentation and so is found in small quantities in some beers and wines, in particular fruit wines. The amount found in wine is pharmacologically insignificant and not sufficient to produce psychoactive effects.[83]

GHB has at least two distinct binding sites[84] in the central nervous system. GHB is an agonist at the newly characterized GHB receptor, which is excitatory,[85][86] and it is a weak agonist at the GABAB receptor, which is inhibitory.[86] GHB is a naturally occurring substance that acts in a similar fashion to some neurotransmitters in the mammalian brain.[87] GHB is probably synthesized from GABA in GABAergic neurons, and released when the neurons fire.[86]

GHB induces the accumulation of either a derivative of tryptophan or tryptophan itself in the extracellular space, possibly by increasing tryptophan transport across the blood–brain barrier. The blood content of certain neutral amino-acids, including tryptophan, is also increased by peripheral GHB administration. GHB-induced stimulation of tissue serotonin turnover may be due to an increase in tryptophan transport to the brain and in its uptake by serotonergic cells. As the serotonergic system may be involved in the regulation of sleep, mood, and anxiety, the stimulation of this system by high doses of GHB may be involved in certain neuropharmacological events induced by GHB administration.

However, at therapeutic doses, GHB reaches much higher concentrations in the brain and activates GABAB receptors, which are primarily responsible for its sedative effects.[90] GHB's sedative effects are blocked by GABAB antagonists.

The role of the GHB receptor in the behavioural effects induced by GHB is more complex. GHB receptors are densely expressed in many areas of the brain, including the cortex and hippocampus, and these are the receptors that GHB displays the highest affinity for. There has been somewhat limited research into the GHB receptor; however, there is evidence that activation of the GHB receptor in some brain areas results in the release of glutamate, the principal excitatory neurotransmitter.[79] Drugs that selectively activate the GHB receptor cause absence seizures in high doses, as do GHB and GABA(B) agonists.[91]

Activation of both the GHB receptor and GABA(B) is responsible for the addictive profile of GHB. GHB's effect on dopamine release is biphasic.[92] Low concentrations stimulate dopamine release via the GHB receptor.[93] Higher concentrations inhibit dopamine release via GABA(B) receptors as do other GABA(B) agonists such as baclofen and phenibut.[94] After an initial phase of inhibition, dopamine release is then increased via the GHB receptor. Both the inhibition and increase of dopamine release by GHB are inhibited by opioid antagonists such as naloxone and naltrexone. Dynorphin may play a role in the inhibition of dopamine release via kappa opioid receptors.[95]

This explains the paradoxical mix of sedative and stimulatory properties of GHB, as well as the so-called "rebound" effect, experienced by individuals using GHB as a sleeping agent, wherein they awake suddenly after several hours of GHB-induced deep sleep. That is to say that, over time, the concentration of GHB in the system decreases below the threshold for significant GABAB receptor activation and activates predominantly the GHB receptor, leading to wakefulness.

Recently, analogs of GHB, such as 4-hydroxy-4-methylpentanoic acid (UMB68) have been synthesised and tested on animals, in order to gain a better understanding of GHB's mode of action.[96] Analogues of GHB such as 3-methyl-GHB, 4-methyl-GHB, and 4-phenyl-GHB have been shown to produce similar effects to GHB in some animal studies, but these compounds are even less well researched than GHB itself. Of these analogues, only 4-methyl-GHB (γ-hydroxyvaleric acid, GHV) and a prodrug form γ-valerolactone (GVL) have been reported as drugs of abuse in humans, and on the available evidence seem to be less potent but more toxic than GHB, with a particular tendency to cause nausea and vomiting.

Other prodrug ester forms of GHB have also rarely been encountered by law enforcement, including 1,4-butanediol diacetate (BDDA/DABD), methyl-4-acetoxybutanoate (MAB), and ethyl-4-acetoxybutanoate (EAB),[citation needed] but these are, in general, covered by analogue laws in jurisdictions where GHB is illegal, and little is known about them beyond their delayed onset and longer duration of action. The intermediate compound γ-hydroxybutyraldehyde (GHBAL) is also a prodrug for GHB; however, as with all aliphatic aldehydes this compound is caustic and is strong-smelling and foul-tasting; actual use of this compound as an intoxicant is likely to be unpleasant and result in severe nausea and vomiting.

Metabolic pathway of GHB.

Both of the metabolic breakdown pathways shown for GHB can run in either direction, depending on the concentrations of the substances involved, so the body can make its own GHB either from GABA or from succinic semialdehyde. Under normal physiological conditions, the concentration of GHB in the body is rather low, and the pathways would run in the reverse direction to what is shown here to produce endogenous GHB. However, when GHB is consumed for recreational or health promotion purposes, its concentration in the body is much higher than normal, which changes the enzyme kinetics so that these pathways operate to metabolise GHB rather than producing it.

Synthesis of the chemical GHB was first reported in 1874 by Alexander Zaytsev,[97] but the first major research into its use in humans was conducted in the early 1960s by Dr. Henri Laborit to use in studying the neurotransmitter GABA.[98] It quickly found a wide range of uses due to its minimal side-effects and short duration of action, the only difficulties being the narrow therapeutic dosage range and the dangers presented by its combination with alcohol and other nervous system depressants.

GHB was widely used in France, Italy, and other European countries for several decades as a sleeping agent and an anesthetic in childbirth but problems with its abuse potential and development of newer drugs have led to a decrease in legitimate medical use of GHB in recent times. In the Netherlands, GHB could be bought as aphrodisiac and euphoriant in a smartshop for several years, until several incidents caused it to become regulated. The only common medical applications for GHB today are in the treatment of narcolepsy and more rarely alcoholism. In the typical scenario, GHB has been synthesized from γ-butyrolactone (GBL) by adding sodium hydroxide (lye) in ethanol or water.

A popular children's toy, Bindeez (also known as Aqua Dots, in the United States), produced by Melbourne company Moose, was banned in Australia in early November 2007 when it was discovered that 1,4-butanediol (1,4-B), which is metabolized into GHB, had been substituted for the non-toxic plasticiser 1,5-pentanediol in the bead manufacturing process. Three young children were hospitalized as a result of ingesting a large number of the beads, and the toy was recalled.[99]

In the UK GHB was made a class C drug in June 2003. In October 2013 the ACMD recommended upgrading it from schedule IV to schedule II in line with UN recommendations. Their report concluded that the minimal use of Xyrem in the UK meant that prescribers would be minimally inconvenienced by the rescheduling.[102] This advice was followed and GHB was moved to schedule 2 on 7 January 2015.[103][104]

In Hong Kong, GHB is regulated under Schedule 1 of Hong Kong's Chapter 134 Dangerous Drugs Ordinance. It can only be used legally by health professionals and for university research purposes. The substance can be given by pharmacists under a prescription. Anyone who supplies the substance without prescription can be fined HK$10,000. The penalty for trafficking or manufacturing the substance is a HK$150,000 fine and life imprisonment. Possession of the substance for consumption without license from the Department of Health is illegal with a HK$100,000 fine or 5 years of jail time.

In New Zealand and Australia, GHB, 1,4-B and GBL are all Class B illegal drugs, along with any possible esters, ethers and aldehydes. GABA itself is also listed as an illegal drug in these jurisdictions, which seems unusual given its failure to cross the blood–brain barrier, but there was a perception among legislators that all known analogues should be covered as far as this was possible. Attempts to circumvent the illegal status of GHB have led to the sale of derivatives such as 4-methyl-GHB (γ-hydroxyvaleric acid, GHV) and its prodrug form γ-valerolactone (GVL), but these are also covered under the law by virtue of their being "substantially similar" to GHB or GBL and; so importation, sale, possession and use of these compounds is also considered to be illegal.

In Chile, GHB is a controlled drug under the law Ley de substancias psicotrópicas y estupefacientes (psychotropic substances and narcotics).

^Department of Health and Human Services, SAMHSA Office of Applied Studies 2005 National Survey on Drug Use and Health (ages 12 years and up); American Heart Association; Johns Hopkins University study, Principles of Addiction Medicine; Psychology Today; National Gambling Impact Commission Study; National Council on Problem Gambling; Illinois Institute for Addiction Recovery; Society for Advancement of Sexual Health; All Psych Journal

1.
Intravenous therapy
–
Intravenous therapy is the infusion of liquid substances directly into a vein. Intravenous infusions are commonly referred to as drips, the intravenous route is the fastest way to deliver fluids and medications throughout the body. Intravenous therapy may be used for administration, to correct electrolyte imbalances, to deliver medications. IVs can be categorized by type of vein the tube inserted, called the catheter. A peripheral IV is used on peripheral veins and this is the most common type of IV therapy used. Central IV lines have their catheters that are advanced through a vein and empty into a central vein, usually the superior vena cava. Other advantages are that because it empties near the heart, medications can also be distributed to the rest of the body. As there is room for multiple parallel compartments within the catheter, caregivers can also measure central venous pressure and other physiological variables through the line. They are also longer, which as reflected in Poiseuilles law, requires higher pressure to achieve the same flow, central IV lines carry risks of bleeding, infection, gangrene, thromboembolism and gas embolism. Surrounding structures such as the pleura and carotid artery are also at risk of damage with the potential for pneumothorax or even cannulation of the artery. There are several types of central IVs, depending on the route that the catheter takes from the outside of the body to the vein, typical uses for a PICC include, long chemotherapy regimens, extended antibiotic therapy, or total parenteral nutrition. This is usually done by measuring the distance to a landmark, such as the suprasternal notch. An X-ray must be used to verify that the tip is in the place when fluoroscopy was not used during the insertion. A PICC may have a tube and connector, two or three compartments, each with its own external connector. Power-injectable PICCs are now available as well, from the outside, a single-lumen PICC resembles a peripheral IV, except that the tubing is slightly wider. The insertion site requires better protection than that of a peripheral IV, however, a PICC poses less of a systemic infection risk than other central IVs, because the insertion site is usually cooler and dryer than the sites typically used for other central lines. This helps to slow the growth of bacteria which could reach the bloodstream by traveling under the skin along the outside of the catheter, although special training is required, a PICC does not require the skill level of a physician or surgeon. It is also externally unobtrusive, and with proper hygiene and care can be left in place for months to years if needed for patients who require extended treatment, also, as a PICC travels through the axilla, it can become kinked, causing poor function

2.
Regulation of therapeutic goods
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The regulation of therapeutic goods, that is drugs and therapeutic devices, varies by jurisdiction. In some countries, such as the United States, they are regulated at the level by a single agency. In other jurisdictions they are regulated at the level, or at both state and national levels by various bodies, as is the case in Australia. The role of therapeutic goods regulation is designed mainly to protect the health, regulation is aimed at ensuring the safety, quality, and efficacy of the therapeutic goods which are covered under the scope of the regulation. In most jurisdictions, therapeutic goods must be registered before they are allowed to be marketed, there is usually some degree of restriction of the availability of certain therapeutic goods depending on their risk to consumers. Therapeutic goods in Australia are regulated by the Therapeutic Goods Administration, there are 5 main categories, Normal Medicines - Cough, cold and fever medicines, antiseptics, vitamins and others. Sold freely in pharmacies and some large supermarkets, red Stripe Medicines - These medicines are sold only with medical prescription. Antibiotics, Anti allergenics, Anti inflammatories, and other medicines, in Brazil, governmental control is loose on this type, it is not uncommon to buy this type of prescription medicine over the counter without a prescription. Red Stripe Psychoactive Medicines - These medicines are only with a Special Control white medical prescription with carbon copy. The original must be retained by the pharmacist after the sale, Drugs include anti-depressants, anti-convulsants, some sleep aids, anti-psychotics and other non-habit-inducing controlled medicines. Though some consider them habit inducing, anabolic steroids are also regulated under this category, black Stripe Medicines - These medicines are sold only with the Blue B Form medical prescription, which is valid for 30 days and must be retained by the pharmacist after the sale. Includes sedatives, some anorexic inducers and other habit-inducing controlled medicines, includes amphetamines and other stimulants, opioids and other strong habit-forming controlled medicines. In Canada, regulation of goods are governed by the Food and Drug Act. In addition, the Controlled Drugs and Substances Act requires additional regulatory requirements for controlled drugs, the regulation of drugs in Burma is governed by the Food and Drug Administration and Food and Drug Board of Authority. The regulation of drugs in China is governed by the China Food, Medicines for Human Use in the United Kingdom are regulated by the Medicines and Healthcare products Regulatory Agency. The availability of drugs is regulated by classification by the MHRA as part of marketing authorisation of a product, Medicines in the Republic of Ireland are regulated according to the Misuse of Drugs Regulations 1988. Controlled drugs are divided into five categories based on their potential for misuse, cD1, cannabis, lysergamide, coca leaf, etc. Use prohibited except in limited circumstances where a license has been granted, CD2, amphetamine, methadone, morphine, fentanyl, oxycodone, tapentadol, etc

3.
Misuse of Drugs Act 1975
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The Misuse of Drugs Act 1975 is a New Zealand drug control law that classifies drugs into three classes, or schedules, based on their projected risk of serious harm of loss of life. The Controlled Substances Classification system has been around for decades but only in 2006 was benzylpiperazine was classified that a substance first became scheduled for health reasons. Most of the controlled substances, such as opium, cocaine. During this conference, the United States were strongly advocating for the banning of these substances unless a scientific or medical use became apparent. New Zealand signed this treaty and its 37th Parliament went on to incorporate this law into the Misuse of Drugs Act 1975, however, the United States did not sign the treaty. ^Note 2, Temazepam and flunitrazepam are subject to legal restrictions. The Expert Advisory Committee on Drugs makes scheduling decisions, based on scientific, national Drug Policy New Zealand notes, The Conventions place certain obligations on signatory countries. When the UN classifies a substance under one of the above Conventions, accordingly, the impetus for some of the drugs to be considered by the EACD will originate from decisions made at the UN

4.
Controlled Substances Act
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The Controlled Substances Act is the statute establishing federal U. S. drug policy under which the manufacture, importation, possession, use and distribution of certain substances is regulated. It was passed by the 91st United States Congress as Title II of the Comprehensive Drug Abuse Prevention and Control Act of 1970, the Act also served as the national implementing legislation for the Single Convention on Narcotic Drugs. The legislation created five Schedules, with varying qualifications for a substance to be included in each, classification decisions are required to be made on criteria including potential for abuse, currently accepted medical use in treatment in the United States, and international treaties. The nation first outlawed addictive drugs in the early 1900s and the International Opium Convention helped lead international agreements regulating trade, the Food and Drugs Act of 1906 was the beginning of over 200 laws concerning public health and consumer protections. Others were the Federal Food, Drug, and Cosmetic Act, in 1969, President Richard Nixon announced that the Attorney General, John N. Shafer—to study cannabis abuse in the United States. It implies an overwhelming indictment of the behavior which we believe is not appropriate, the actual and potential harm of use of the drug is not great enough to justify intrusion by the criminal law into private behavior, a step which our society takes only with the greatest reluctance. According to David T. Courtwright, the Act was part of a reform package designed to rationalize. It eliminated mandatory minimum sentences and provided support for drug treatment, king notes that the rehabilitation clauses were added as a compromise to Senator Jim Hughes, who favored a moderate approach. The bill, as introduced by Senator Everett Dirksen, ran to 91 pages, since its enactment in 1970, the Act has been amended several times, The Medical Device Amendments of 1976. The Psychotropic Substances Act of 1978 added provisions implementing the Convention on Psychotropic Substances, the Controlled Substances Penalties Amendments Act of 1984. The Ryan Haight Online Pharmacy Consumer Protection Act of 2008 The Electronic Prescriptions for Controlled Substances 2010, the Controlled Substances Act consists of 2 subchapters. Subchapter II describes the laws for exportation and importation of controlled substances, again specifying fines, the Drug Enforcement Administration was established in 1973, combining the Bureau of Narcotics and Dangerous Drugs and Customs drug agents. When a petition is received by the DEA, the agency begins its own investigation of the drug and this request is sent to the Assistant Secretary of Health of HHS. Under certain circumstances, the Government may temporarily schedule a drug without following the normal procedure, an example is when international treaties require control of a substance. In addition,21 U. S. C. §811 allows the Attorney General to temporarily place a substance in Schedule I to avoid an imminent hazard to the public safety, in any case, once these proceedings are complete, the temporary order is automatically vacated. Unlike ordinary scheduling proceedings, such orders are not subject to judicial review. The CSA also creates a system of distribution for those authorized to handle controlled substances. The cornerstone of this system is the registration of all those authorized by the DEA to handle controlled substances

5.
Netherlands
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The Netherlands is the main constituent country of the Kingdom of the Netherlands. It is a densely populated country located in Western Europe with three territories in the Caribbean. The European part of the Netherlands borders Germany to the east, Belgium to the south, and the North Sea to the northwest, sharing borders with Belgium, the United Kingdom. The three largest cities in the Netherlands are Amsterdam, Rotterdam and The Hague, Amsterdam is the countrys capital, while The Hague holds the Dutch seat of parliament and government. The port of Rotterdam is the worlds largest port outside East-Asia, the name Holland is used informally to refer to the whole of the country of the Netherlands. Netherlands literally means lower countries, influenced by its low land and flat geography, most of the areas below sea level are artificial. Since the late 16th century, large areas have been reclaimed from the sea and lakes, with a population density of 412 people per km2 –507 if water is excluded – the Netherlands is classified as a very densely populated country. Only Bangladesh, South Korea, and Taiwan have both a population and higher population density. Nevertheless, the Netherlands is the worlds second-largest exporter of food and agricultural products and this is partly due to the fertility of the soil and the mild climate. In 2001, it became the worlds first country to legalise same-sex marriage, the Netherlands is a founding member of the EU, Eurozone, G-10, NATO, OECD and WTO, as well as being a part of the Schengen Area and the trilateral Benelux Union. The first four are situated in The Hague, as is the EUs criminal intelligence agency Europol and this has led to the city being dubbed the worlds legal capital. The country also ranks second highest in the worlds 2016 Press Freedom Index, the Netherlands has a market-based mixed economy, ranking 17th of 177 countries according to the Index of Economic Freedom. It had the thirteenth-highest per capita income in the world in 2013 according to the International Monetary Fund, in 2013, the United Nations World Happiness Report ranked the Netherlands as the seventh-happiest country in the world, reflecting its high quality of life. The Netherlands also ranks joint second highest in the Inequality-adjusted Human Development Index, the region called Low Countries and the country of the Netherlands have the same toponymy. Place names with Neder, Nieder, Nether and Nedre and Bas or Inferior are in use in all over Europe. They are sometimes used in a relation to a higher ground that consecutively is indicated as Upper, Boven, Oben. In the case of the Low Countries / the Netherlands the geographical location of the region has been more or less downstream. The geographical location of the region, however, changed over time tremendously

6.
Pharmacokinetics
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Pharmacokinetics, sometimes abbreviated as PK, is a branch of pharmacology dedicated to determining the fate of substances administered to a living organism. The substances of interest include any chemical xenobiotic such as, pharmaceutical drugs, pesticides, food additives, cosmetic ingredients, etc. It attempts to analyze chemical metabolism and to discover the fate of a chemical from the moment that it is administered up to the point at which it is eliminated from the body. Pharmacokinetics is the study of how an organism affects a drug, both together influence dosing, benefit, and adverse effects, as seen in PK/PD models. Pharmacokinetic properties of chemicals are affected by the route of administration and these may affect the absorption rate. Models have been developed to simplify conceptualization of the processes that take place in the interaction between an organism and a chemical substance. The various compartments that the model is divided into are commonly referred to as the ADME scheme, absorption - the process of a substance entering the blood circulation. Distribution - the dispersion or dissemination of substances throughout the fluids, metabolism – the recognition by the organism that a foreign substance is present and the irreversible transformation of parent compounds into daughter metabolites. Excretion - the removal of the substances from the body, in rare cases, some drugs irreversibly accumulate in body tissue. The two phases of metabolism and excretion can also be grouped together under the title elimination, the study of these distinct phases involves the use and manipulation of basic concepts in order to understand the process dynamics. All these concepts can be represented through mathematical formulas that have a graphical representation. The model outputs for a drug can be used in industry or in the application of pharmacokinetic concepts. Clinical pharmacokinetics provides many performance guidelines for effective and efficient use of drugs for human-health professionals, in practice, it is generally considered that steady state is reached when a time of 4 to 5 times the half-life for a drug after regular dosing is started. Noncompartmental methods estimate the exposure to a drug by estimating the area under the curve of a concentration-time graph, compartmental methods estimate the concentration-time graph using kinetic models. Noncompartmental methods are more versatile in that they do not assume any specific compartmental model. The final outcome of the transformations that a drug undergoes in an organism, a number of functional models have been developed in order to simplify the study of pharmacokinetics. These models are based on a consideration of an organism as a number of related compartments, the simplest idea is to think of an organism as only one homogenous compartment. However, these models do not always reflect the real situation within an organism

7.
Bioavailability
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By definition, when a medication is administered intravenously, its bioavailability is 100%. However, when a medication is administered via other routes, its bioavailability generally decreases or may vary from patient to patient, Bioavailability is one of the essential tools in pharmacokinetics, as bioavailability must be considered when calculating dosages for non-intravenous routes of administration. Bioavailability is defined differently for drugs as opposed to dietary supplements primarily due to the method of administration and Food. Bioaccessibility is a related to bioavailability in the context of biodegradation. A molecule is said to be bioaccessible when is available to cross a cellular membrane from the environment. In pharmacology, bioavailability is a measurement of the rate and extent to which a drug reaches at the site of action and it is denoted by the letter f. Therefore, bioavailability for dietary supplements can be defined as the proportion of the administered substance capable of being absorbed, in both pharmacology and nutrition sciences, bioavailability is measured by calculating the area under curve of the drug concentration time profile. Bioavailability is commonly a factor in the production of crops. Toxic materials in soil, such as lead from paint may be rendered unavailable to animals ingesting contaminated soil by supplying phosphorus fertilizers in excess and it is the fraction of the drug absorbed through non-intravenous administration compared with the corresponding intravenous administration of the same drug. The comparison must be normalized, consequently, the amount absorbed is corrected by dividing the corresponding dose administered. The absolute bioavailability is the area under curve non-intravenous divided by AUC intravenous. For example, the formula for calculating F for a drug administered by the route is given below. If we compare the two different dosage forms having same active ingredients and compare the two drug bioavailability is called comparative bioavailability, although knowing the true extent of systemic absorption is clearly useful, in practice it is not determined as frequently as one may think. The reason for this is that its assessment requires a reference, that is. These limitations may be overcome, however, by administering a low dose of an isotopically labelled drug concomitantly with a therapeutic non-labelled oral dose. This technique eliminates pharmacokinetic issues on non-equivalent clearance as well as enabling the intravenous dose to be administered with a minimum of toxicology, the technique was first applied using stable-isotopes such as 13C and mass-spectrometry to distinguish the isotopes by mass difference. More recently, 14C labelled drugs are administered intravenously and accelerator mass spectrometry used to measure the isotopically labelled drug along with mass spectrometry for the unlabelled drug, in all such cases, to conduct an absolute bioavailability study requires that the drug be given intravenously. Intravenous administration of a drug can provide valuable information on the fundamental pharmacokinetic parameters of volume of distribution

8.
Drug metabolism
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Drug metabolism is the metabolic breakdown of drugs by living organisms, usually through specialized enzymatic systems. These pathways are a form of biotransformation present in all groups of organisms. These reactions often act to detoxify poisonous compounds, the study of drug metabolism is called pharmacokinetics. The metabolism of drugs is an important aspect of pharmacology. For example, the rate of metabolism determines the duration and intensity of a drugs pharmacologic action, the enzymes of xenobiotic metabolism, particularly the glutathione S-transferases are also important in agriculture, since they may produce resistance to pesticides and herbicides. Drug metabolism is divided into three phases, in phase I, enzymes such as cytochrome P450 oxidases introduce reactive or polar groups into xenobiotics. These modified compounds are conjugated to polar compounds in phase II reactions. These reactions are catalysed by enzymes such as glutathione S-transferases. Finally, in phase III, the conjugated xenobiotics may be processed, before being recognised by efflux transporters. Drug metabolism often converts lipophilic compounds into hydrophilic products that are readily excreted. The exact compounds an organism is exposed to will be unpredictable, and may differ widely over time. The solution that has evolved to address this problem is an elegant combination of physical barriers, all organisms use cell membranes as hydrophobic permeability barriers to control access to their internal environment. This selective uptake means that most hydrophilic molecules cannot enter cells, in contrast, the diffusion of hydrophobic compounds across these barriers cannot be controlled, and organisms, therefore, cannot exclude lipid-soluble xenobiotics using membrane barriers. However, the existence of a permeability barrier means that organisms were able to evolve detoxification systems that exploit the hydrophobicity common to membrane-permeable xenobiotics and these systems therefore solve the specificity problem by possessing such broad substrate specificities that they metabolise almost any non-polar compound. Useful metabolites are excluded since they are polar, and in general one or more charged groups. However, since these compounds are few in number, specific enzymes can recognize, the metabolism of xenobiotics is often divided into three phases, - modification, conjugation, and excretion. These reactions act in concert to detoxify xenobiotics and remove them from cells, in phase I, a variety of enzymes act to introduce reactive and polar groups into their substrates. One of the most common modifications is hydroxylation catalysed by the cytochrome P-450-dependent mixed-function oxidase system and these enzyme complexes act to incorporate an atom of oxygen into nonactivated hydrocarbons, which can result in either the introduction of hydroxyl groups or N-, O- and S-dealkylation of substrates

9.
Excretion
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Excretion is the process by which metabolic wastes and other non-useful materials are eliminated from an organism. In vertebrates this is carried out by the lungs, kidneys. This is in contrast with secretion, where the substance may have specific tasks after leaving the cell, excretion is an essential process in all forms of life. For example, in urine is expelled through the urethra. In unicellular organisms, waste products are discharged directly through the surface of the cell, green plants produce carbon dioxide and water as respiratory products. In green plants, the carbon dioxide released during respiration gets utilized during photosynthesis, oxygen is a by product generated during photosynthesis, and exits through stomata, root cell walls, and other routes. Plants can get rid of water by transpiration and guttation. These latter processes do not need added energy, they act passively, however, during the pre-abscission phase, the metabolic levels of a leaf are high. Plants also excrete some waste substances into the soil around them, in animals, the main excretory products are carbon dioxide, ammonia, urea, uric acid, guanine and creatine. The liver and kidneys clear many substances from the blood, aquatic animals usually excrete ammonia directly into the external environment, as this compound has high solubility and there is ample water available for dilution. In terrestrial animals ammonia-like compounds are converted into other materials as there is less water in the environment. Birds excrete their nitrogenous wastes as uric acid in the form of a paste and this is metabolically more expensive, but allows more efficient water retention and it can be stored more easily in the egg. Many avian species, especially seabirds, can also excrete salt via specialized nasal salt glands, in insects, a system involving Malpighian tubules is utilized to excrete metabolic waste. Metabolic waste diffuses or is actively transported into the tubule, which transports the wastes to the intestines, the metabolic waste is then released from the body along with fecal matter. The excreted material may be called dejecta or ejecta, in pathology the word ejecta is more commonly used. UAlberta. ca, Animation of excretion Brian J Ford on leaf fall in Nature

10.
PubChem
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PubChem is a database of chemical molecules and their activities against biological assays. The system is maintained by the National Center for Biotechnology Information, a component of the National Library of Medicine, PubChem can be accessed for free through a web user interface. Millions of compound structures and descriptive datasets can be downloaded via FTP. PubChem contains substance descriptions and small molecules with fewer than 1000 atoms and 1000 bonds, more than 80 database vendors contribute to the growing PubChem database. PubChem consists of three dynamically growing primary databases, as of 28 January 2016, Compounds,82.6 million entries, contains pure and characterized chemical compounds. Substances,198 million entries, contains also mixtures, extracts, complexes, bioAssay, bioactivity results from 1.1 million high-throughput screening programs with several million values. PubChem contains its own online molecule editor with SMILES/SMARTS and InChI support that allows the import and export of all common chemical file formats to search for structures and fragments. In the text search form the database fields can be searched by adding the name in square brackets to the search term. A numeric range is represented by two separated by a colon. The search terms and field names are case-insensitive, parentheses and the logical operators AND, OR, and NOT can be used. AND is assumed if no operator is used, example,0,5000,50,10 -5,5 PubChem was released in 2004. The American Chemical Society has raised concerns about the publicly supported PubChem database and they have a strong interest in the issue since the Chemical Abstracts Service generates a large percentage of the societys revenue. To advocate their position against the PubChem database, ACS has actively lobbied the US Congress, soon after PubChems creation, the American Chemical Society lobbied U. S. Congress to restrict the operation of PubChem, which they asserted competes with their Chemical Abstracts Service

11.
Guide to Pharmacology
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The IUPHAR/BPS Guide to PHARMACOLOGY is an open-access website, acting as a portal to information on the biological targets of licensed drugs and other small molecules. The Guide to PHARMACOLOGY is developed as a joint venture between the International Union of Basic and Clinical Pharmacology and the British Pharmacological Society and this replaces and expands upon the original 2009 IUPHAR Database. The information featured includes pharmacological data, target and gene nomenclature, overviews and commentaries on each target family are included, with links to key references. The Guide to PHARMACOLOGY was initially made available online in December 2011 with additional material released in July 2012 and its network of over 700 specialist advisors contribute expertise and data. The current PI and Grant holder of the GtoPdb project is Prof. Jamie A. Davies, the development and release of the first version of the GtoPdb in 2012 was described in an editorial published in the British Journal of Pharmacology entitled Guide to Pharmacology. org- an update. The IUPHAR-DB is no longer being developed and all the contained within this site is now available through the Guide to PHARMACOLOGY. A complete list of all the approved drugs included on the website is available via the ligand list. The Guide to PHARMACOLOGY is being expanded to include information on targets and ligands. Search features on the website include quick and advanced search options, other features include Hot topic news items and a recent receptor-ligand pairing list. A hard copy summary of the database is published as The Concise Guide to Pharmacology 2015/2016 as a series of papers as a bi-annual supplement to the British Journal of Pharmacology. The Guide to PHARMACOLOGY includes links to other relevant resources via target, many of these resources maintain reciprocal links with the relevant Guide to PHARMACOLOGY pages. As of November 2015 the Wellcome Trust is supporting a new project to develop the Guide to Immumopharmacology, the latter continues to be supported by the British Pharmacological Society

12.
DrugBank
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The DrugBank database is a comprehensive, freely accessible, online database containing information on drugs and drug targets. As both a bioinformatics and a resource, DrugBank combines detailed drug data with comprehensive drug target information. Because of its scope, comprehensive referencing and unusually detailed data descriptions. As a result, links to DrugBank are maintained for nearly all drugs listed in Wikipedia, DrugBank is widely used by the drug industry, medicinal chemists, pharmacists, physicians, students and the general public. Its extensive drug and drug-target data has enabled the discovery and repurposing of a number of existing drugs to treat rare, the latest release of the database contains 8227 drug entries including 2003 FDA-approved small molecule drugs,221 FDA-approved biotech drugs,93 nutraceuticals and over 6000 experimental drugs. Additionally,4270 non-redundant protein sequences are linked to these drug entries, each DrugCard entry contains more than 200 data fields with half of the information being devoted to drug/chemical data and the other half devoted to drug target or protein data. Four additional databases, HMDB, T3DB, SMPDB and FooDB are also part of a suite of metabolomic/cheminformatic databases. The first version of DrugBank was released in 2006 and this early release contained relatively modest information about 841 FDA-approved small molecule drugs and 113 biotech drugs. It also included information on 2133 drug targets, the second version of DrugBank was released in 2009. This greatly expanded and improved version of the database included 1344 approved small molecule drugs and 123 biotech drugs as well as 3037 unique drug targets. Version 2.0 also included, for the first time, withdrawn drugs and illicit drugs, version 3.0 was released in 2011. This version contained 1424 approved small molecule drugs and 132 biotech drugs as well as >4000 unique drug targets, version 3.0 also included drug transporter data, drug pathway data, drug pricing, patent and manufacturing data as well as data on >5000 experimental drugs. Version 4.0 was released in 2014 and this version included 1558 FDA-approved small molecule drugs,155 biotech drugs and 4200 unique drug targets. Version 4.0 also incorporated information on drug metabolites, drug taxonomy, drug spectra, drug binding constants. Table 1 provides a complete statistical summary of the history of DrugBank’s development. All data in DrugBank is non-proprietary or is derived from a non-proprietary source and it is freely accessible and available to anyone. In addition, nearly every item is fully traceable and explicitly referenced to the original source. DrugBank data is available through a web interface and downloads

13.
ChemSpider
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ChemSpider is a database of chemicals. ChemSpider is owned by the Royal Society of Chemistry, the database contains information on more than 50 million molecules from over 500 data sources including, Each chemical is given a unique identifier, which forms part of a corresponding URL. This is an approach to develop an online chemistry database. The search can be used to widen or restrict already found results, structure searching on mobile devices can be done using free apps for iOS and for the Android. The ChemSpider database has been used in combination with text mining as the basis of document markup. The result is a system between chemistry documents and information look-up via ChemSpider into over 150 data sources. ChemSpider was acquired by the Royal Society of Chemistry in May,2009, prior to the acquisition by RSC, ChemSpider was controlled by a private corporation, ChemZoo Inc. The system was first launched in March 2007 in a release form. ChemSpider has expanded the generic support of a database to include support of the Wikipedia chemical structure collection via their WiChempedia implementation. A number of services are available online. SyntheticPages is an interactive database of synthetic chemistry procedures operated by the Royal Society of Chemistry. Users submit synthetic procedures which they have conducted themselves for publication on the site and these procedures may be original works, but they are more often based on literature reactions. Citations to the published procedure are made where appropriate. They are checked by an editor before posting. The pages do not undergo formal peer-review like a journal article. The comments are moderated by scientific editors. The intention is to collect practical experience of how to conduct useful chemical synthesis in the lab, while experimental methods published in an ordinary academic journal are listed formally and concisely, the procedures in ChemSpider SyntheticPages are given with more practical detail. Comments by submitters are included as well, other publications with comparable amounts of detail include Organic Syntheses and Inorganic Syntheses

14.
ChEMBL
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ChEMBL or ChEMBLdb is a manually curated chemical database of bioactive molecules with drug-like properties. It is maintained by the European Bioinformatics Institute, of the European Molecular Biology Laboratory, based at the Wellcome Trust Genome Campus, Hinxton, the database, originally known as StARlite, was developed by a biotechnology company called Inpharmatica Ltd. later acquired by Galapagos NV. The data was acquired for EMBL in 2008 with an award from The Wellcome Trust, resulting in the creation of the ChEMBL chemogenomics group at EMBL-EBI, the ChEMBL database contains compound bioactivity data against drug targets. Bioactivity is reported in Ki, Kd, IC50, and EC50, data can be filtered and analyzed to develop compound screening libraries for lead identification during drug discovery. ChEMBL version 2 was launched in January 2010, including 2.4 million bioassay measurements covering 622,824 compounds and this was obtained from curating over 34,000 publications across twelve medicinal chemistry journals. ChEMBLs coverage of available bioactivity data has grown to become the most comprehensive ever seen in a public database, in October 2010 ChEMBL version 8 was launched, with over 2.97 million bioassay measurements covering 636,269 compounds. ChEMBL_10 saw the addition of the PubChem confirmatory assays, in order to integrate data that is comparable to the type, ChEMBLdb can be accessed via a web interface or downloaded by File Transfer Protocol. It is formatted in a manner amenable to computerized data mining, ChEMBL is also integrated into other large-scale chemistry resources, including PubChem and the ChemSpider system of the Royal Society of Chemistry. In addition to the database, the ChEMBL group have developed tools and these include Kinase SARfari, an integrated chemogenomics workbench focussed on kinases. The system incorporates and links sequence, structure, compounds and screening data, the primary purpose of ChEMBL-NTD is to provide a freely accessible and permanent archive and distribution centre for deposited data. July 2012 saw the release of a new data service, sponsored by the Medicines for Malaria Venture. The data in this service includes compounds from the Malaria Box screening set, myChEMBL, the ChEMBL virtual machine, was released in October 2013 to allow users to access a complete and free, easy-to-install cheminformatics infrastructure. In December 2013, the operations of the SureChem patent informatics database were transferred to EMBL-EBI, in a portmanteau, SureChem was renamed SureChEMBL. 2014 saw the introduction of the new resource ADME SARfari - a tool for predicting and comparing cross-species ADME targets

15.
Chemical formula
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These are limited to a single typographic line of symbols, which may include subscripts and superscripts. A chemical formula is not a name, and it contains no words. Although a chemical formula may imply certain simple chemical structures, it is not the same as a full chemical structural formula. Chemical formulas can fully specify the structure of only the simplest of molecules and chemical substances, the simplest types of chemical formulas are called empirical formulas, which use letters and numbers indicating the numerical proportions of atoms of each type. Molecular formulas indicate the numbers of each type of atom in a molecule. For example, the formula for glucose is CH2O, while its molecular formula is C6H12O6. This is possible if the relevant bonding is easy to show in one dimension, an example is the condensed molecular/chemical formula for ethanol, which is CH3-CH2-OH or CH3CH2OH. For reasons of structural complexity, there is no condensed chemical formula that specifies glucose, chemical formulas may be used in chemical equations to describe chemical reactions and other chemical transformations, such as the dissolving of ionic compounds into solution. A chemical formula identifies each constituent element by its chemical symbol, in empirical formulas, these proportions begin with a key element and then assign numbers of atoms of the other elements in the compound, as ratios to the key element. For molecular compounds, these numbers can all be expressed as whole numbers. For example, the formula of ethanol may be written C2H6O because the molecules of ethanol all contain two carbon atoms, six hydrogen atoms, and one oxygen atom. Some types of compounds, however, cannot be written with entirely whole-number empirical formulas. An example is boron carbide, whose formula of CBn is a variable non-whole number ratio with n ranging from over 4 to more than 6.5. When the chemical compound of the consists of simple molecules. These types of formulas are known as molecular formulas and condensed formulas. A molecular formula enumerates the number of atoms to reflect those in the molecule, so that the formula for glucose is C6H12O6 rather than the glucose empirical formula. However, except for very simple substances, molecular chemical formulas lack needed structural information, for simple molecules, a condensed formula is a type of chemical formula that may fully imply a correct structural formula. For example, ethanol may be represented by the chemical formula CH3CH2OH

16.
Simplified molecular-input line-entry system
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The simplified molecular-input line-entry system is a specification in form of a line notation for describing the structure of chemical species using short ASCII strings. SMILES strings can be imported by most molecule editors for conversion back into two-dimensional drawings or three-dimensional models of the molecules, the original SMILES specification was initiated in the 1980s. It has since modified and extended. In 2007, a standard called OpenSMILES was developed in the open-source chemistry community. Other linear notations include the Wiswesser Line Notation, ROSDAL and SLN, the original SMILES specification was initiated by David Weininger at the USEPA Mid-Continent Ecology Division Laboratory in Duluth in the 1980s. The Environmental Protection Agency funded the project to develop SMILES. It has since modified and extended by others, most notably by Daylight Chemical Information Systems. In 2007, a standard called OpenSMILES was developed by the Blue Obelisk open-source chemistry community. Other linear notations include the Wiswesser Line Notation, ROSDAL and SLN, in July 2006, the IUPAC introduced the InChI as a standard for formula representation. SMILES is generally considered to have the advantage of being slightly more human-readable than InChI, the term SMILES refers to a line notation for encoding molecular structures and specific instances should strictly be called SMILES strings. However, the term SMILES is also used to refer to both a single SMILES string and a number of SMILES strings, the exact meaning is usually apparent from the context. The terms canonical and isomeric can lead to confusion when applied to SMILES. The terms describe different attributes of SMILES strings and are not mutually exclusive, typically, a number of equally valid SMILES strings can be written for a molecule. For example, CCO, OCC and CC all specify the structure of ethanol, algorithms have been developed to generate the same SMILES string for a given molecule, of the many possible strings, these algorithms choose only one of them. This SMILES is unique for each structure, although dependent on the algorithm used to generate it. These algorithms first convert the SMILES to a representation of the molecular structure. A common application of canonical SMILES is indexing and ensuring uniqueness of molecules in a database, there is currently no systematic comparison across commercial software to test if such flaws exist in those packages. SMILES notation allows the specification of configuration at tetrahedral centers, and these are structural features that cannot be specified by connectivity alone and SMILES which encode this information are termed isomeric SMILES

17.
International Chemical Identifier
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Initially developed by IUPAC and NIST from 2000 to 2005, the format and algorithms are non-proprietary. The continuing development of the standard has supported since 2010 by the not-for-profit InChI Trust. The current version is 1.04 and was released in September 2011, prior to 1.04, the software was freely available under the open source LGPL license, but it now uses a custom license called IUPAC-InChI Trust License. Not all layers have to be provided, for instance, the layer can be omitted if that type of information is not relevant to the particular application. InChIs can thus be seen as akin to a general and extremely formalized version of IUPAC names and they can express more information than the simpler SMILES notation and differ in that every structure has a unique InChI string, which is important in database applications. Information about the 3-dimensional coordinates of atoms is not represented in InChI, the InChI algorithm converts input structural information into a unique InChI identifier in a three-step process, normalization, canonicalization, and serialization. The InChIKey, sometimes referred to as a hashed InChI, is a fixed length condensed digital representation of the InChI that is not human-understandable. The InChIKey specification was released in September 2007 in order to facilitate web searches for chemical compounds and it should be noted that, unlike the InChI, the InChIKey is not unique, though collisions can be calculated to be very rare, they happen. In January 2009 the final 1.02 version of the InChI software was released and this provided a means to generate so called standard InChI, which does not allow for user selectable options in dealing with the stereochemistry and tautomeric layers of the InChI string. The standard InChIKey is then the hashed version of the standard InChI string, the standard InChI will simplify comparison of InChI strings and keys generated by different groups, and subsequently accessed via diverse sources such as databases and web resources. Every InChI starts with the string InChI= followed by the version number and this is followed by the letter S for standard InChIs. The remaining information is structured as a sequence of layers and sub-layers, the layers and sub-layers are separated by the delimiter / and start with a characteristic prefix letter. The six layers with important sublayers are, Main layer Chemical formula and this is the only sublayer that must occur in every InChI. The atoms in the formula are numbered in sequence, this sublayer describes which atoms are connected by bonds to which other ones. Describes how many hydrogen atoms are connected to each of the other atoms, the condensed,27 character standard InChIKey is a hashed version of the full standard InChI, designed to allow for easy web searches of chemical compounds. Most chemical structures on the Web up to 2007 have been represented as GIF files, the full InChI turned out to be too lengthy for easy searching, and therefore the InChIKey was developed. With all databases currently having below 50 million structures, such duplication appears unlikely at present, a recent study more extensively studies the collision rate finding that the experimental collision rate is in agreement with the theoretical expectations. Example, Morphine has the structure shown on the right, as the InChI cannot be reconstructed from the InChIKey, an InChIKey always needs to be linked to the original InChI to get back to the original structure

18.
Neurotransmitter
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Neurotransmitters, also known as chemical messengers, are endogenous chemicals that enable neurotransmission. They transmit signals across a synapse, such as a neuromuscular junction, from one neuron to another target neuron, muscle cell. Neurotransmitters are released from synaptic vesicles in synapses into the synaptic cleft, neurotransmitters play a major role in shaping everyday life and functions. Their exact numbers are unknown, but more than 100 chemical messengers have been uniquely identified, neurotransmitters are stored in a synapse in synaptic vesicles, clustered beneath the membrane in the axon terminal located at the presynaptic side of the synapse. Neurotransmitters are released into and diffused across the cleft, where they bind to specific receptors in the membrane on the postsynaptic side of the synapse. Most neurotransmitters are about the size of an amino acid, however. Nevertheless, short-term exposure of the receptor to a neurotransmitter is typically sufficient for causing a postsynaptic response by way of synaptic transmission, in response to a threshold action potential or graded electrical potential, a neurotransmitter is released at the presynaptic terminal. Low level baseline release also occurs without electrical stimulation, the released neurotransmitter may then move across the synapse to be detected by and bind with receptors in the postsynaptic neuron. Binding of neurotransmitters may influence the postsynaptic neuron in either an inhibitory or excitatory way and this neuron may be connected to many more neurons, and if the total of excitatory influences are greater than those of inhibitory influences, the neuron will also fire. Ultimately it will create a new action potential at its axon hillock to release neurotransmitters, until the early 20th century, scientists assumed that the majority of synaptic communication in the brain was electrical. However, through the careful histological examinations by Ramón y Cajal, upon completion of this experiment, Loewi asserted that sympathetic regulation of cardiac function can be mediated through changes in chemical concentrations. Furthermore, Otto Loewi is credited with discovering acetylcholine —the first known neurotransmitter, some neurons do, however, communicate via electrical synapses through the use of gap junctions, which allow specific ions to pass directly from one cell to another. There are four criteria for identifying neurotransmitters, The chemical must be synthesized in the neuron or otherwise be present in it. When the neuron is active, the chemical must be released, the same response must be obtained when the chemical is experimentally placed on the target. A mechanism must exist for removing the chemical from its site of activation after its work is done, have little or no effect on membrane voltage, but have a common carrying function such as changing the structure of the synapse. Communicate by sending messages that affect the release or reuptake of transmitters. Various techniques and experiments such as staining, stimulating, and collecting can be used to identify throughout the central nervous system. There are many different ways to classify neurotransmitters, dividing them into amino acids, peptides, and monoamines is sufficient for some classification purposes

19.
Psychoactive drug
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A psychoactive drug, psychopharmaceutical, or psychotropic is a chemical substance that changes brain function and results in alterations in perception, mood, or consciousness. These substances may be used recreationally, to alter ones consciousness, or, as entheogens, for ritual, spiritual, or shamanic purposes. Some categories of drugs, which have medical therapeutic value, are prescribed by medical doctors. There are also some psychoactive substances used in the detoxification and rehabilitation programs for drug users. Psychoactive substances often bring about changes in consciousness and mood that the user may find rewarding. In addition, sustained use of some substances may produce a physical dependence or psychological dependence syndrome associated with somatic or psychological-emotional withdrawal states respectively, Drug rehabilitation aims to break this cycle of dependency, through a combination of psychotherapy, support groups, maintenance and even other psychoactive substances. However, the reverse is true in some cases, that certain experiences on drugs may be so unfriendly. This is especially true of certain deliriants, powerful dissociatives, and classic psychedelics, in part because of this potential for substance misuse, addiction, or dependence, the ethics of drug use is debated. Restrictions on drug production and sales in an attempt to drug abuse are very common among national and sub-national governments worldwide. Ethical concerns have also raised about over-use of these drugs clinically. Psychoactive drug use can be traced to prehistory, there is archaeological evidence of the use of psychoactive substances dating back at least 10,000 years, and historical evidence of cultural use over the past 5,000 years. The chewing of coca leaves, for example, dates back over 8,000 years ago in Peruvian society, medicinal use is one important facet of psychoactive drug usage. However, some have postulated that the urge to alter ones consciousness is as primary as the drive to satiate thirst, hunger or sexual desire. Supporters of this belief contend that the history of use and even childrens desire for spinning, swinging. It is, however, necessary to precisely what is meant by the use of drugs. We do not mean the purely physical craving, but there are not many drugs which have the power of stilling such craving. This relationship is not limited to humans, a number of animals consume different psychoactive plants, animals, berries and even fermented fruit, becoming intoxicated, such as cats after consuming catnip. Traditional legends of sacred plants often contain references to animals that introduced humankind to their use, animals and psychoactive plants appear to have co-evolved, possibly explaining why these chemicals and their receptors exist within the nervous system

20.
Glycine
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Glycine is the amino acid that has a single hydrogen atom as its side chain. It is the simplest possible amino acid, the chemical formula of glycine is NH2‐CH2‐COOH. Glycine is one of the amino acids. Its codons are GGU, GGC, GGA, GGG of the genetic code, Glycine is a colorless, sweet-tasting crystalline solid. It is unique among the amino acids in that it is achiral. It can fit into hydrophilic or hydrophobic environments since it exists as zwitterion at natural pH, Glycine was first isolated from gelatin in 1820. The name comes from the ancient Greek word γλυκύς sweet tasting, Glycine was discovered in 1820, by Henri Braconnot who boiled a gelatinous object with sulfuric acid. Glycine is manufactured industrially by treating chloroacetic acid with ammonia, ClCH2COOH +2 NH3 → H2NCH2COOH + NH4Cl About 15 million kg are produced annually in this way, in the USA and in Japan, glycine is produced via the Strecker amino acid synthesis. Glycine is also cogenerated as an impurity in the synthesis of EDTA, arising from reactions of the ammonia coproduct. In aqueous solution, glycine itself is amphoteric, at low pH the molecule can be protonated with a pKa of about 2.4, the nature of glycine in aqueous solution has been investigated by theoretical methods. In solution the ratio of concentrations of the two isomers is independent of both the concentration and of pH. This ratio is simply the equilibrium constant for isomerization, K = / Both isomers of glycine have been observed by microwave spectroscopy in the gas phase. The solid-state structure has been analyzed in detail and this conversion is readily reversible, CO2 + NH+4 + N5, N10-Methylene tetrahydrofolate + NADH + H+ → Glycine + tetrahydrofolate + NAD+ Glycine is coded by codons GGU, GGC, GGA and GGG. Most proteins incorporate only small quantities of glycine, a notable exception is collagen, which contains about 35% glycine. Glycine is degraded via three pathways, the first step is the reverse of glycine biosynthesis from serine with serine hydroxymethyl transferase. Serine is then converted to pyruvate by serine dehydratase, in the third pathway of glycine degradation, glycine is converted to glyoxylate by D-amino acid oxidase. Glyoxylate is then oxidized by lactate dehydrogenase to oxalate in an NAD+-dependent reaction. The half-life of glycine and its elimination from the body varies significantly based on dose, in one study, the half-life was between 0.5 and 4.0 hours

21.
GABA receptor
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The GABA receptors are a class of receptors that respond to the neurotransmitter gamma-aminobutyric acid, the chief inhibitory compound in the mature vertebrate central nervous system. GABA receptors influence cognition by coordinating with glutamatergic processes, there are two classes of GABA receptors, GABAA and GABAB. GABAA receptors are ligand-gated ion channels, whereas GABAB receptors are G protein-coupled receptors and it has long been recognized that the fast response of neurons to GABA that is blocked by bicuculline and picrotoxin is due to direct activation of an anion channel. This channel was subsequently termed the GABAA receptor, fast-responding GABA receptors are members of a family of Cys-loop ligand-gated ion channels. In ionotropic GABAA receptors, binding of GABA molecules to their sites in the extracellular part of the receptor triggers opening of a chloride ion-selective pore. The increased chloride conductance drives the membrane potential towards the potential of the Cl¯ ion which is about –65 mV in neurons. This mechanism is responsible for the effects of GABAA allosteric agonists. In addition, activation of GABA receptors lead to the so-called shunting inhibition, there have been numerous reports of excitatory GABAA receptors. According to the excitatory GABA theory, this phenomenon is due to increased intracellular concentration of Cl¯ ions either during development of the system or in certain cell populations. After this period of development, a pump is upregulated and inserted into the cell membrane. Further openings via GABA binding to the receptor then produce inhibitory responses, over-excitation of this receptor induces receptor remodeling and the eventual invagination of the GABA receptor. As a result, further GABA binding becomes inhibited and inhibitory postsynaptic potentials are no longer relevant, a subclass of ionotropic GABA receptors, insensitive to typical allosteric modulators of GABAA receptor channels such as benzodiazepines and barbiturates, was designated GABAС receptor. Native responses of the GABAC receptor type occur in retinal bipolar or horizontal cells across vertebrate species, GABAС receptors are exclusively composed of ρ subunits that are related to GABAA receptor subunits. Although the term GABAС receptor is used, GABAС may be viewed as a variant within the GABAA receptor family. Others have argued that the differences between GABAС and GABAA receptors are large enough to justify maintaining the distinction between these two subclasses of GABA receptors, a slow response to GABA is mediated by GABAB receptors, originally defined on the basis of pharmacological properties. In studies focused on the control of neurotransmitter release, it was noted that a GABA receptor was responsible for modulating evoked release in a variety of isolated tissue preparations. The most striking discovery was the finding that baclofen, a clinically employed spasmolytic mimicked, in a stereoselective manner, later ligand-binding studies provided direct evidence of binding sites for baclofen on central neuronal membranes. CDNA cloning confirmed that the GABAB receptor belongs to the family of G-protein coupled receptors, additional information on GABAB receptors has been reviewed elsewhere

Intravenous therapy
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Intravenous therapy is the infusion of liquid substances directly into a vein. Intravenous infusions are commonly referred to as drips, the intravenous route is the fastest way to deliver fluids and medications throughout the body. Intravenous therapy may be used for administration, to correct electrolyte imbalances, to deliver medications. IVs can

Regulation of therapeutic goods
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The regulation of therapeutic goods, that is drugs and therapeutic devices, varies by jurisdiction. In some countries, such as the United States, they are regulated at the level by a single agency. In other jurisdictions they are regulated at the level, or at both state and national levels by various bodies, as is the case in Australia. The role of

1.
Methylphenidate, in the form of Ritalin pills.

Misuse of Drugs Act 1975
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The Misuse of Drugs Act 1975 is a New Zealand drug control law that classifies drugs into three classes, or schedules, based on their projected risk of serious harm of loss of life. The Controlled Substances Classification system has been around for decades but only in 2006 was benzylpiperazine was classified that a substance first became scheduled

1.
Misuse of Drugs Act 1975

Controlled Substances Act
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The Controlled Substances Act is the statute establishing federal U. S. drug policy under which the manufacture, importation, possession, use and distribution of certain substances is regulated. It was passed by the 91st United States Congress as Title II of the Comprehensive Drug Abuse Prevention and Control Act of 1970, the Act also served as the

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Regulation of therapeutic goods in the United States

2.
Controlled Substances Act

Netherlands
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The Netherlands is the main constituent country of the Kingdom of the Netherlands. It is a densely populated country located in Western Europe with three territories in the Caribbean. The European part of the Netherlands borders Germany to the east, Belgium to the south, and the North Sea to the northwest, sharing borders with Belgium, the United K

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The Netherlands in 5500 BC

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Flag

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The Netherlands in 500 BC

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An oak figurine found in Willemstad, North Brabant (4500 BC).

Pharmacokinetics
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Pharmacokinetics, sometimes abbreviated as PK, is a branch of pharmacology dedicated to determining the fate of substances administered to a living organism. The substances of interest include any chemical xenobiotic such as, pharmaceutical drugs, pesticides, food additives, cosmetic ingredients, etc. It attempts to analyze chemical metabolism and

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Different forms of tablets, which will have different pharmacokinetic behaviours after their administration.

2.
Graph that demonstrates the Michaelis-Menten kinetics model for the relationship between an enzyme and a substrate: one of the parameters studies in pharmacokinetics, where the substrate is a pharmaceutical drug.

Bioavailability
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By definition, when a medication is administered intravenously, its bioavailability is 100%. However, when a medication is administered via other routes, its bioavailability generally decreases or may vary from patient to patient, Bioavailability is one of the essential tools in pharmacokinetics, as bioavailability must be considered when calculati

1.
Absolute bioavailability is a ratio of areas under the curves. IV, intravenous; PO, oral route.

Drug metabolism
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Drug metabolism is the metabolic breakdown of drugs by living organisms, usually through specialized enzymatic systems. These pathways are a form of biotransformation present in all groups of organisms. These reactions often act to detoxify poisonous compounds, the study of drug metabolism is called pharmacokinetics. The metabolism of drugs is an i

1.
Cytochrome P450 oxidases are important enzymes in xenobiotic metabolism.

Excretion
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Excretion is the process by which metabolic wastes and other non-useful materials are eliminated from an organism. In vertebrates this is carried out by the lungs, kidneys. This is in contrast with secretion, where the substance may have specific tasks after leaving the cell, excretion is an essential process in all forms of life. For example, in u

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White cast of uric acid defecated with the dark feces from a lizard. Insects, birds and some other reptiles also undergo a similar mechanism.

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Chemical structure of uric acid.

PubChem
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PubChem is a database of chemical molecules and their activities against biological assays. The system is maintained by the National Center for Biotechnology Information, a component of the National Library of Medicine, PubChem can be accessed for free through a web user interface. Millions of compound structures and descriptive datasets can be dow

1.
PubChem

Guide to Pharmacology
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The IUPHAR/BPS Guide to PHARMACOLOGY is an open-access website, acting as a portal to information on the biological targets of licensed drugs and other small molecules. The Guide to PHARMACOLOGY is developed as a joint venture between the International Union of Basic and Clinical Pharmacology and the British Pharmacological Society and this replace

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IUPHAR/BPS Guide to Pharmacology

DrugBank
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The DrugBank database is a comprehensive, freely accessible, online database containing information on drugs and drug targets. As both a bioinformatics and a resource, DrugBank combines detailed drug data with comprehensive drug target information. Because of its scope, comprehensive referencing and unusually detailed data descriptions. As a result

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Fig. 1. DrugBank DrugCard

ChemSpider
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ChemSpider is a database of chemicals. ChemSpider is owned by the Royal Society of Chemistry, the database contains information on more than 50 million molecules from over 500 data sources including, Each chemical is given a unique identifier, which forms part of a corresponding URL. This is an approach to develop an online chemistry database. The

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ChemSpider

ChEMBL
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ChEMBL or ChEMBLdb is a manually curated chemical database of bioactive molecules with drug-like properties. It is maintained by the European Bioinformatics Institute, of the European Molecular Biology Laboratory, based at the Wellcome Trust Genome Campus, Hinxton, the database, originally known as StARlite, was developed by a biotechnology company

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Centres and institutes

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ChEMBL

Chemical formula
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These are limited to a single typographic line of symbols, which may include subscripts and superscripts. A chemical formula is not a name, and it contains no words. Although a chemical formula may imply certain simple chemical structures, it is not the same as a full chemical structural formula. Chemical formulas can fully specify the structure of

1.
Al 2 (SO 4) 3

Simplified molecular-input line-entry system
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The simplified molecular-input line-entry system is a specification in form of a line notation for describing the structure of chemical species using short ASCII strings. SMILES strings can be imported by most molecule editors for conversion back into two-dimensional drawings or three-dimensional models of the molecules, the original SMILES specifi

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Generation of SMILES: Break cycles, then write as branches off a main backbone. (Ciprofloxacin)

International Chemical Identifier
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Initially developed by IUPAC and NIST from 2000 to 2005, the format and algorithms are non-proprietary. The continuing development of the standard has supported since 2010 by the not-for-profit InChI Trust. The current version is 1.04 and was released in September 2011, prior to 1.04, the software was freely available under the open source LGPL lic

1.
L - ascorbic acid

Neurotransmitter
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Neurotransmitters, also known as chemical messengers, are endogenous chemicals that enable neurotransmission. They transmit signals across a synapse, such as a neuromuscular junction, from one neuron to another target neuron, muscle cell. Neurotransmitters are released from synaptic vesicles in synapses into the synaptic cleft, neurotransmitters pl

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The synthesis, packaging, secretion, and removal of neurotransmitters.

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Postsynaptic density

Psychoactive drug
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A psychoactive drug, psychopharmaceutical, or psychotropic is a chemical substance that changes brain function and results in alterations in perception, mood, or consciousness. These substances may be used recreationally, to alter ones consciousness, or, as entheogens, for ritual, spiritual, or shamanic purposes. Some categories of drugs, which hav

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An assortment of psychoactive drugs - street drugs and medications

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Alcohol is a widely used and abused psychoactive drug. The global alcoholic drinks industry is expected to exceed $1 trillion this year. Beer is the third-most popular drink overall, after water and tea.

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Zoloft (sertraline) is an SSRI antidepressant.

4.
Timothy Leary was a leading proponent of spiritual hallucinogen use.

Glycine
–
Glycine is the amino acid that has a single hydrogen atom as its side chain. It is the simplest possible amino acid, the chemical formula of glycine is NH2‐CH2‐COOH. Glycine is one of the amino acids. Its codons are GGU, GGC, GGA, GGG of the genetic code, Glycine is a colorless, sweet-tasting crystalline solid. It is unique among the amino acids in

GABA receptor
–
The GABA receptors are a class of receptors that respond to the neurotransmitter gamma-aminobutyric acid, the chief inhibitory compound in the mature vertebrate central nervous system. GABA receptors influence cognition by coordinating with glutamatergic processes, there are two classes of GABA receptors, GABAA and GABAB. GABAA receptors are ligand

2.
Alcohol is a widely used and abused psychoactive drug. The global alcoholic drinks industry is expected to exceed $1 trillion this year. Beer is the third-most popular drink overall, after water and tea.

3.
Zoloft (sertraline) is an SSRI antidepressant.

4.
Timothy Leary was a leading proponent of spiritual hallucinogen use.

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Top view of a module base (lid removed) looking into the four separated wells where cell culture inserts would usually sit and be exposed to tobacco smoke or an aerosol for an in-vitro study of the effects.

1.
All forms of the recovery position share basic principles. The mouth is downward so that fluid can drain from the patient's airway; the chin is well up to keep the epiglottis opened. Arms and legs are locked to stabilize the position of the patient